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Originally published In Press as doi:10.1074/jbc.M210429200 on March 6, 2003

J. Biol. Chem., Vol. 278, Issue 19, 17036-17043, May 9, 2003
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Stimulation of Airway Mucin Gene Expression by Interleukin (IL)-17 through IL-6 Paracrine/Autocrine Loop*

Yin ChenDagger , Philip ThaiDagger , Yu-Hua ZhaoDagger , Ye-Shih Ho§, Mary M. DeSouza, and Reen WuDagger ||

From the Dagger  Center for Comparative Respiratory Biology and Medicine and Division of Pulmonary and Critical Care Medicine, University of California, Davis, California 95616, § Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan 48201, and  GlaxoSmithKline Pharmaceuticals, King of Prussia, Pennsylvania 19406

Mucus hypersecretion and persistent airway inflammation are common features of various airway diseases, such as asthma, chronic obstructive pulmonary disease, and cystic fibrosis. One key question is: does the associated airway inflammation in these diseases affect mucus production? If so, what is the underlying mechanism? It appears that increased mucus secretion results from increased mucin gene expression and is also frequently accompanied by an increased number of mucous cells (goblet cell hyperplasia/metaplasia) in the airway epithelium. Many studies on mucin gene expression have been directed toward Th2 cytokines such as interleukin (IL)-4, IL-9, and IL-13 because of their known pathophysiological role in allergic airway diseases such as asthma. However, the effect of these cytokines has not been definitely linked to their direct interaction with airway epithelial cells. In our study, we treated highly differentiated cultures of primary human tracheobronchial epithelial (TBE) cells with a panel of cytokines (interleukin-1alpha , 1beta , 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 15, 16, 17, 18, and tumor necrosis factor alpha ). We found that IL-6 and IL-17 could stimulate the mucin genes, MUC5B and MUC5AC. The Th2 cytokines IL-4, IL-9, and IL-13 did not stimulate MUC5AC or MUC5B in our experiments. A similar stimulation of MUC5B/Muc5b expression by IL-6 and IL-17 was demonstrated in primary monkey and mouse TBE cells. Further investigation of MUC5B expression demonstrated that IL-17's effect is at least partly mediated through IL-6 by a JAK2-dependent autocrine/paracrine loop. Finally, evidence is presented to show that both IL-6 and IL-17 mediate MUC5B expression through the ERK signaling pathway.

* This work was supported by National Institutes of Health Grants HL35635, ES06230, ES09701, AI50496, ES00628, ES04699, and ES05707, California Tobacco-Related Disease Research Program 10RT-0262, and a grant from Glaxo/Smith Kline/Welcome Inc.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

|| To whom correspondence should be addressed: Center for Comparative Respiratory Biology and Medicine, Surge 1 Annex, Room 1121, University of California at Davis, One Shields Ave., Davis, CA 95616. Tel.: 530-752-2648; Fax: 530-752-8632; E-mail: rwu@ucdavis.edu.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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